Abstract: A thin steel sheet has a steel structure which has a ferrite area fraction of 30% or less, a bainite area fraction of 5% or less, a martensite and tempered martensite area fraction of 70% or more, and a retained austenite area fraction of 2.0% or less and in which the ratio of the dislocation density in the range of 0 ?m to 20 ?m from a surface of the steel sheet to the dislocation density of a through-thickness central portion of the steel sheet is 90% to 110% and the average of the top 10% of the sizes of cementite grains located in a depth of up to 100 ?m from a surface of the steel sheet is 300 nm or less. The maximum camber of the steel sheet sheared to a length of 1 m in a longitudinal direction of the steel sheet is 15 mm or less.

Abstract: Postoperative adhesion formation at an invasion site and migration of neutrophils to the site of surgical invasion are suppressed by administering an anti-IL-6 receptor antibody and/or a neutrophil-neutralizing antibody.

Abstract: Based on the identification of IL-33 as an exacerbating factor in endometriosis and adenomyosis uteri, a method for treating or alleviating endometriosis or adenomyosis uteri, involves administering an IL-33 antagonist, which is capable of inhibiting the function of IL-33. The IL-33 antagonist is useful for treating, preventing or alleviating endometriosis and uterine adenomyosis uteri.

Abstract: Based on the identification of IL-33 as an exacerbating factor in endometriosis and adenomyosis uteri, a therapeutic agent for endometriosis and adenomyosis uteri has an IL-33 antagonist, which is capable of inhibiting the function of IL-33. The IL-33 antagonist is useful for treating, preventing or alleviating endometriosis and uterine adenomyosis uteri.

Abstract: Postoperative adhesion formation at an invasion site and migration of neutrophils to the site of surgical invasion are suppressed by administering an anti-IL-6 receptor antibody and/or a neutrophil-neutralizing antibody.

Abstract: Based on the identification of IL-33 as an exacerbating factor in endometriosis and adenomyosis uteri, a therapeutic agent for endometriosis and adenomyosis uteri has an IL-33 antagonist, which is capable of inhibiting the function of IL-33. The IL-33 antagonist is useful for treating, preventing or alleviating endometriosis and uterine adenomyosis uteri.

Abstract: The present invention provides a transgenic non-human mammal retaining, in a specifically expressible state, a DNA encoding IL-33 in the skin, and having one or more features selected from the group consisting of (1) spontaneous onset of dermatitis, (2) increase in the number of inflammatory cells, (3) increase in total IgE concentration, histamine concentration, cytokine concentration and/or chemokine concentration, and (4) increase in scratching time, under SPF (specific pathogen free) breeding conditions, as compared to a corresponding non-transgenic non-human mammal, and the like.

Abstract: The present invention provides a transgenic non-human mammal retaining, in a specifically expressible state, a DNA encoding IL-33 in the skin, and having one or more features selected from the group consisting of (1) spontaneous onset of dermatitis, (2) increase in the number of inflammatory cells, (3) increase in total IgE concentration, histamine concentration, cytokine concentration and/or chemokine concentration, and (4) increase in scratching time, under SPF (specific pathogen free) breeding conditions, as compared to a corresponding non-transgenic non-human mammal, and the like.

Abstract: The present invention provides a complex of an antigen and IgE binding to the antigen, a composition including an antigen and IgE binding to the antigen, and a method of using the complex or the composition to screen candidate therapeutics for TH-2 type diseases, for example in animal models.

Abstract: The present invention provides a complex of an antigen and IgE binding to the antigen, a composition including an antigen and IgE binding to the antigen, and a method of using the complex or the composition. With the present invention, it is possible to induce naive T cells to develop into Th2 cells. Moreover, the present invention clarified a working mechanism of a Th2-type immune response, particularly a production mechanism of early IL-4. With use of the present invention, it is possible to provide a technique of treating and preventing Th2-type diseases.